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Impairments of inhibitory circuits are at the basis of most, if not all, cognitive deficits. The impact of OPHN1, a gene associate with intellectual disability (ID), on inhibitory neurons remains elusive. We addressed this issue by analyzing the postnatal migration of inhibitory interneurons derived from the subventricular zone in a validated mouse model of ID (OPHN1 -/y mice). We found that the speed and directionality of migrating neuroblasts were deeply perturbed in OPHN1 -/y mice. The significant reduction in speed was due to altered chloride (Cl - ) homeostasis, while the overactivation of the OPHN1 downstream signaling pathway, RhoA kinase (ROCK), caused abnormalities in the directionality of the neuroblast progression in mutants. Blocking the cation-Cl - cotransporter KCC2 almost completely rescued the migration speed while proper directionality was restored upon ROCK inhibition. Our data unveil a strong impact of OPHN1 on GABAergic inhibitory interneurons and identify putative targets for successful therapeutic approaches.

Altered Cl − homeostasis hinders forebrain GABAergic interneuron migration in a mouse model of intellectual disability

Altered Cl ⁻ homeostasis hinders forebrain GABAergic interneuron migration in a mouse model of intellectual disability